Histone deacetylases in memory and cognition

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Science Signaling  09 Dec 2014:
Vol. 7, Issue 355, pp. re12
DOI: 10.1126/scisignal.aaa0069

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  • HDAC- and HAT-targeted therapies in neurodegenerative diseases
    • Ranjeet Singh Mahla, Ph.D. student, Indian Institute of Science Education and Research, Bhopal, India

    The recent review article by Penny et al. 2014 (10.1126/scisignal.aaa0069) concludes that histone deacetylase (HDAC) inhibitor treatment is promising to ameliorate the pathological consequences of neurological disorders such as Alzheimers disease (AD). Basically the article emphasizes the importance of histone acetylation in cognitive learning, where functional regulation of HDAC2 is very important. Inhibition of HDACs leads to enhanced histone acetyl transferase (HAT) activity, which has been considered as central for brain development. A study published in the Journal of Neuroscience by Chatterjee et al. in 2013 (10.1523/JNEUROSCI.5772-12.2013) has demonstrated that the synthetic small molecule CSP-TTK21 activates CBP/p300, which promotes neurogenesis and ultimately leads to memory extension. So, both promotion of HATs and inhibition of HDACs can enhance neurogenesis and can be implicated in therapy. However, it is known that these epigenetic regulators regulate diverse aspects of organisms' development and are involved in disease progression so, it is indeed important to understand how HDACs and HATs can be targeted in a context-specific manner without compromising normal physiological functions.

    Competing Interests: None declared.

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